Evidence map›Paper›PMID 32918152›Full record

ReviewCurrent diabetes reports2020

Mechanisms of Congenital Malformations in Pregnancies with Pre-existing Diabetes.

Mary R Loeken

Open access · greenAbstract readReview
In one paragraph

Review in Current diabetes reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  14. Systems biology analysis of human genomes points to key pathways conferring spina bifida risk.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Article
  16. Review
  17. Skeletal malformations and growth disturbances in fetuses of mild diabetic ratsBiomedica : revista del Instituto Nacional de Salud · 2021
    Article
  18. Article
  19. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Mary R LoekenSection on Islet Cell and Regenerative Biology, Department of Medicine, Joslin Diabetes Center and Harvard Medical School, One Joslin Place, Boston, MA, 02215, USA. Mary.loeken@joslin.harvard.edu.
Harvard University · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
SEARCH FOR THE MOLECULAR CAUSES OF DIABETIC EMBRYOPATHYR01DK052865 · NIDDK · JOSLIN DIABETES CENTER · PI LOEKEN, MARY R · 1998 to 2013
$4.4M
MOLECULAR REGULATION: EMBYROGENESIS BY METABOLIC STRESSR01DK058300 · NIDDK · JOSLIN DIABETES CENTER · PI LOEKEN, MARY R · 2000 to 2014
$4.3M
Role of Slc2a2/Glut2 in Embryo and Stem Cell Metabolism, Self-Renewal, and Pathways Involved in Diabetic EmbryopathyR01DK104649 · NIDDK · JOSLIN DIABETES CENTER · PI LOEKEN, MARY R · 2015 to 2018
$2.1M
NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R01 DK052865NIDDK NIH HHS R01 DK058300NIDDK NIH HHS R01 DK104649
6 · The paper itself

Abstract

purpose of reviewFetuses of diabetic mothers are at increased risk for congenital malformations. Research in recent decades using animal and embryonic stem cell models has revealed many embryonic developmental processes that are disturbed by maternal diabetes. The aim of this review is to give clinicians a better understanding of the reasons for rigorous glycemic control in early pregnancy, and to provide background to guide future research. RECENT

findingsMouse models of diabetic pregnancy have revealed mechanisms for altered expression of tissue-specific genes that lead to malformations that are more common in diabetic pregnancies, such as neural tube defects (NTDs) and congenital heart defects (CHDs), and how altered gene expression causes apoptosis that leads to malformations. Embryos express the glucose transporter, GLUT2, which confers susceptibility to malformation, due to high rates of glucose uptake during maternal hyperglycemia and subsequent oxidative stress; however, the teleological function of GLUT2 for mammalian embryos may be to transport the amino sugar glucosamine (GlcN) from maternal circulation to be used as substrate for glycosylation reactions and to promote embryo cell growth. Malformations in diabetic pregnancy may be not only due to excess glucose uptake but also due to insufficient GlcN uptake. Avoiding maternal hyperglycemia during early pregnancy should prevent excess glucose uptake via GLUT2 into embryo cells, and also permit sufficient GLUT2-mediated GlcN uptake.

Indexed as

Diabetes, GestationalHyperglycemiaNeural Tube DefectsPregnancy in DiabeticsAnimalsFemaleHumansMiceOxidative StressPregnancyDiabetic embryopathyDiabetic pregnancyHyperglycemia in pregnancyNeural tube defectsOxidative stress in pregnancyPax3

Identifiers

PMID32918152
PMCPMC7803009
OpenAlexW3085614497

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.